Herbicides resistance mechanisms

Chemical, cultural, and mechanical weed control practices have been relatively successful ia reducing yield losses from weeds (448). However, herbicide-resistant weed populations, soil erosion, pesticide persistence ia the environment, and other problems associated with technologies used (ca 1993) to control weeds have raised concerns for the long-term efficacy and sustainability of herbicide-dependent crop production practices (449). These concerns, coupled with ever-increasing demands for food and fiber, contribute to the need for innovative weed management strategies (450). 

The high efficacy of triazine herbicides and their repetitive use in crops and noncrop situations has resulted in the selection of weeds that are resistant to these herbicides or are not well controlled at the lower rates now being used. In most instances, triazine resistance is due to an alteration in the herbicide-binding site in PS II. Despite the widespread occurrence of triazine resistance, these herbicides are still widely used, even in fields in which triazine-resistant biotypes are known to occur. The rate of increase in the selection for triazine-resistant weed species depends in part on the integration of alternative weed control strategies, in addition to the use of triazine herbicides, for control of these weed species. Due to their resistance mechanism, many triazine-resistant weeds are less competitive than their susceptible counterparts. 

Sigematsu, Y., F. Sato, and Y. Yamada (1989). The mechanism of herbicide resistance in tobacco cells with a new mutation in the QB protein. Plant Physiol., 89 986-992. 

Multiple-resistance is when more than one mechanism conferring resistance to herbicides in different chemical classes is active in an individual weed or population of weeds. Plants with multiple resistance may possess two or more distinct resistance mechanisms. Two grass species that display both cross- and multiple-resistance are rigid (or annual) ryegrass and blackgrass (Hall et al., 1994). 

Excellent progress has been made in the understanding of the cause, nature, genetics, mechanism and solutions of herbicide-resistant weeds since the first triazine-resistant common groundsel was reported more than 35 years ago. Resistance management programs have been extremely successful in controlling most weeds that have developed resistance to the triazine herbicides. However, research is critical to better understand the rapid increase and spread of many new weed biotypes resistant to several classes of herbicides. 

Hall, L.M., J.A.M. Holtum, and S.B. Powles (1994). Mechanisms responsible for cross resistance and multiple resistance. In S.B. Powles and J.A.M. Holtum, eds., Herbicide Resistance in Plants Biology and Biochemistry. Boca Raton, Florida CRC Press, pp. 243-261. 

Holt, J.S., S.B. Powles, and J.A.M. Holtum (1993). Mechanisms and agronomic aspects of herbicide resistance. Annu. Rev. Plant Physiol., Plant Mol. Biol., 44 203-229. 

Rubin, B. (1996). Herbicide-resistant weeds The inevitable phenomenon Mechanisms, distribution and significance. Z. Pfl. Krankh, Pfl. Schutz, Sonderh., XV 17-32. 

Multiple-resistance mechanisms, defined as resistance due to more than one mode of action or class of herbicide, have been reported in several ALS-resistant weed biotypes - including false cleavers, wild oat, common waterhemp, kochia, rigid ryegrass in Australia (Powles and Matthews, 1992 Preston and Mallory-Smith, 2001), and wild radish (Walsh etal, 2004a). 

Boutsalis, P. (2001). Herbicide Resistance Action Committee (HRAC) Web page http //plantprotection.org/HRAC Bradshaw, L.D., S.R. Padgette, S.L. Kimball, and B.H. Wells (1997). Perspectives on glyphosate resistance. Weed Technol., 11 189-198. Bravin, F., A. Onofri, G. Zanin, and M. Sattin (2004). Is malathion a useful tool to infer the chlorsulfuron-resistance mechanism in mul-tiresistant Italian populations of Lolium spp. 4th International Weed Science Congress, p. 52, S15MT08P00. 

Preston, C. and C.A. Mallory-Smith (2001). Biochemical mechanisms, inheritance, and molecular genetics of herbicide resistance in weeds. In Powles, S.B. and Shaner, D.L., eds., Herbicide Resistance and World Grains. Boca Raton, FL CRC Press, pp. 23-60. 

Saari, L.L., J.C. Cotterman, and M.M. Primiani (1990). Mechanisms of sulfonylurea herbicide resistance in the broadleaf weed Kochia scoparia. Plant Physiol., 93 55-61. 

Shaner, D.L. (1995). Studies on the mechanisms and genetics of resistance Their contribution to herbicide resistance management. Brighton Crop Prot. Conf.Weeds, 2 537-545. 

The use of herbicide rotation to avoid resistance will not be successful in cases where resistance is conferred by non-specific detoxification mechanisms that act on herbicides with different modes of action. In this case, selection for weeds resistant to members of two or more mode-of-action groups can and does occur [9]. Therefore, alternating or rotating amongst herbicides from different mode-of-action groups does necessarily delay resistance development. Clearly, there is no simple herbicide rotation solution to resistance avoidance. The tremendous genetic diversity in some seed populations allows the evolution of resistance, with the resistance mechanism simply reflecting the nature of the selection pressure that was applied. 

One elegant approach to reducing the rate of resistance evolution could be to apply herbicides as mixtures of active partners which cannot be rendered inactive by the same resistance mechanism. This is analogous to the use of drug combinations to ensure broad-sectrum control of susceptible and potentially resistant pathogoi strains. In such a... 

In certain situations it is possible to overcome herbicide metabolism-based resistance by adding an ingredient that will block detoxification of the herbicide in the resistant weed. One example is with propanil-resistant Echinochloa colona in rice in Latin America. The addition of piperophos, an organophosphate insecticide that inhibits the aryl acylamidase activity that confers resistance on the weed biotype [11]. This combination, based on an undo standing of the resistance mechanism, has beat approved for use on resistant... 

Many different bioassays and biochemical or genetic tests have been developed to identify resistant weeds. However, these are normally conducted after the suspected development of resistance, not in a proactive or preventive manner. The potential for evolution of resistance to a new herbicide can be examined in several ways wild-type populations can be screened for resistant individuals, model plant populations can be muta-genized and screened for resistance, resistant cells can be selected in culture, with or without prior exposure to the herbicide, or biochemical or genetic assays can be used to identify known resistance mechanisms. However, more complex or obscure resistance mechanisms may exist, and certain mechanisms may only be expressed in whole plants, not in cell cultures. More recent techniques focused on rapid genetic evolution can also provide a clue to the relative ease with which resistance can be generated, but still require a large investment. However, as in many predictive studies, it is often difficult to relate the results of such experiments to resistance evolution in the field. 

Genetic analysis of different resistant mechanisms against the herbicidal antibiotic... 

Before Radosevich and De Villiers found in 1975 that isolated chloroplasts of resistant common groundsel were insensitive to atrazine and simazine (2), it had been erroneously assumed that all living plants would die if the herbicides could reach their target site intact. We now know that mechanisms of selectivity in crops can be due to differences in metabolism rates, uptake, translocation, site of action or avoidance mechanisms. However, the mechanisms of herbicide resistance that have evolved in weeds are usually different from the mechanisms of herbicide selectivity in most crops. This is certainly true with the most prevalent and thoroughly studied cases of herbicide resistance, including the triazines, dinitroanilines, and AHAS inhibitors. 

While most plants are susceptible to paraquat, some paraquat-resistant horseweed (Erigeron sp. and Conyza sp.) biotypes are apparently insensitive to the herbicide due either to elevated levels of superoxide dismutase and other enzymes in a pathway detoxifying oxygen radicals or to differential sequestration of paraquat in the weed (8, 9). Data on the mechanism of most other types of herbicide resistance in weeds are still not complete. 

Triazine Resistance We attempted to answer the previous four questions using data and examples derived from the study of the best documented case of herbicide resistance, triazine resistance. Two kinds of mechanisms may be responsible for this triazine resistance first is the presence of detoxification metabolic pathways, as seen in corn (11). This also may occur in weed populations, especially Panicoideae, but a low heritability makes its study complex. The second mechanism of triazine resistance is the loss of herbicide binding at the level of the chloroplast. 

Two kinds of resistant biotypes have been noted one is highly-resistant (R) and is unaffected even by saturated solutions of dinitroaniline herbicide, whereas an intermediate-resistant (I) biotype is only 50X resistant to trifluralin and less than 10X resistant to oryzalin compared with the susceptible (S) biotype. Both R and I biotypes are cross-resistant to phosphoric amide herbicides. Tubulin from the R is able to polymerize into microtubules even in the presence of oryzalin, whereas that of the S biotypes cannot. Western blots of tubulin from the R biotype reveal two -tubulin isotypes whereas only one form is noted in the S biotype. Because the R biotype is hypersensitive to the microtubule-stabilizing agent taxol, it is likely that the R biotype is resistant by having hyperstabilized microtubules. The I biotype has no gross alteration in tubulin nor extreme sensitivity to taxol, indicating that this biotype has a different resistance mechanism than the R. 

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